The progression of chronic tuberculosis in the mouse does not require the participation of B lymphocytes or interleukin-4.

The aging process is associated with alterations in the immune system. Some of the changes reported are an increase in the proportion of B lymphocytes, and a shift to a TH2-like cytokine environment. It has been hypothesized that the development of immunopathology within the lung during tuberculosis is linked to increased interleukin-4 (IL-4) production. In addition, a role for B cells in maintaining granuloma integrity has been recently proposed. This study investigated the role of B cells and IL-4 during the long-term course of chronic tuberculosis in mice and showed that the course of Mycobacterium tuberculosis infection in the lungs was not influenced by the absence of B lymphocytes or the TH2 cytokine IL-4.